Document Detail


ACE2, a promising therapeutic target for pulmonary hypertension.
MedLine Citation:
PMID:  21215698     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Pulmonary arterial hypertension (PAH) is a chronic lung disease with poor diagnosis and limited therapeutic options. The currently available therapies are ineffective in improving the quality of life and reducing mortality rates. There exists a clear unmet medical need to treat this disease, which necessitates the discovery of novel therapeutic targets/agents for safe and successful therapy. An altered renin-angiotensin system (RAS) has been implicated as a causative factor in the pathogenesis of PAH. Angiotensin II (Ang II), a key effector peptide of the RAS, can exert deleterious effects on the pulmonary vasculature resulting in vasoconstriction, proliferation, and inflammation, all of which contribute to PAH development. Recently, a new member of the RAS, angiotensin converting enzyme 2 (ACE2), was discovered. This enzyme functions as a negative regulator of the angiotensin system by metabolizing Ang II to a putative protective peptide, angiotensin-(1-7). ACE2 is abundantly expressed in the lung tissue and emerging evidence suggests a beneficial role for this enzyme against lung diseases. In this review, we focus on ACE2 in relation to pulmonary hypertension and provide proof of principle for its therapeutic role in PAH.
Authors:
Vinayak Shenoy; Yanfei Qi; Michael J Katovich; Mohan K Raizada
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Review     Date:  2011-01-05
Journal Detail:
Title:  Current opinion in pharmacology     Volume:  11     ISSN:  1471-4973     ISO Abbreviation:  Curr Opin Pharmacol     Publication Date:  2011 Apr 
Date Detail:
Created Date:  2011-04-12     Completed Date:  2011-08-05     Revised Date:  2012-09-20    
Medline Journal Info:
Nlm Unique ID:  100966133     Medline TA:  Curr Opin Pharmacol     Country:  England    
Other Details:
Languages:  eng     Pagination:  150-5     Citation Subset:  IM    
Copyright Information:
Copyright © 2010 Elsevier Ltd. All rights reserved.
Affiliation:
Department of Physiology and Functional Genomics, University of Florida, Gainesville, FL, USA.
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MeSH Terms
Descriptor/Qualifier:
Angiotensin-Converting Enzyme Inhibitors / therapeutic use*
Animals
Cell Proliferation
Endothelium, Vascular / physiology
Humans
Hypertension, Pulmonary / drug therapy*,  etiology
Inflammation / prevention & control
Muscle, Smooth, Vascular / cytology
Oxidative Stress
Peptidyl-Dipeptidase A / analysis,  physiology*
Ventricular Remodeling
Grant Support
ID/Acronym/Agency:
HL 99980/HL/NHLBI NIH HHS; HL102033/HL/NHLBI NIH HHS; R01 HL056921-14/HL/NHLBI NIH HHS; R01 HL056921-16/HL/NHLBI NIH HHS; R01 HL102033-01/HL/NHLBI NIH HHS; R01 HL102033-02/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Angiotensin-Converting Enzyme Inhibitors; EC 3.4.15.1/Peptidyl-Dipeptidase A; EC 3.4.17.-/angiotensin converting enzyme 2
Comments/Corrections

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